Ultraviolet Keratitis Medication

The goal of ultraviolet (UV) keratitis therapy is to treat the pain associated with damage in the corneal epithelium resulting from UV light exposure and to prevent infection while the cornea heals. Some medications include ophthalmic antibiotics, topical cycloplegics, ophthalmic anesthetics, ophthalmic and parenteral nonsteroidal anti-inflammatory drugs (NSAIDs), and other analgesics.

Class Summary

These agents are indicated for pain relief. Local anesthetics stabilize the neuronal membrane and prevent the initiation and transmission of nerve impulses, thereby producing the local anesthetic action.

Proparacaine 0.5% (Alcaine, Ophthetic)

Has rapid onset of anesthesia that begins 13-30 sec after instillation. However, has short duration of action of about 15-20 min. Since prolonged eye anesthesia can eliminate patient's awareness of mechanical damage to the cornea, drug should not be used outside the ED. Frequent use of anesthetics may retard healing. Least irritating of all topical anesthetics. Prevents initiation and transmission of impulse at nerve cell membrane by stabilizing and decreasing ion permeability.

Class Summary

These agents relax ciliary muscle spasm that can cause a deep aching pain and photophobia. Cycloplegics are used to facilitate eye examination and provide relief of symptoms in patients with moderate-to-severe eye injury. Cycloplegic agents also are mydriatics, thus before using them it is important to ensure that the patient does not have glaucoma. This medication could provoke an acute angle-closure glaucoma attack in a susceptible patient.

Cyclopentolate 0.5-1% (Cyclogyl)

Prevents muscle of ciliary body, and sphincter muscle of iris from responding to cholinergic stimulation. Induces mydriasis in 30-60 min and cycloplegia in 25-75 min.

Class Summary

The routine use of topical antibiotics remains controversial. Many emergency physicians have stopped its use for minor injuries, although others continue routine treatment with a broad-spectrum antibiotic ointment for lubrication and infection prophylaxis. This treatment persists despite its unproven efficacy, discomfort, and evidence that ointments may retard corneal epithelial healing.

Erythromycin ophthalmic (Ilotycin, AK-Mycin)

Indicated for treatment of infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections.

Gentamicin (Genoptic, Garamycin)

Aminoglycoside antibiotic used for gram-negative bacterial coverage.

Class Summary

Although most NSAIDs are used primarily for their anti-inflammatory effects, they are effective analgesics and are useful for the relief of mild to moderate pain. Pain control is essential to quality patient care. Although oral narcotics may be sedating they should be prescribed and are nearly always needed to gain adequate pain control. Prescribing adequate pain medications on the first visit is essential to prevent a revisit solely for pain control. Only a small quantity is needed since this is a self-limited problem with short duration.

Ibuprofen (Motrin, Advil, Nuprin, Rufen)

Usually the DOC for mild to moderate pain, if no contraindications exist; inhibits inflammatory reactions and pain, probably by decreasing cyclooxygenase activity, which results in the inhibition of prostaglandin synthesis

Oxycodone and acetaminophen (Percocet, Tylox, Roxicet)

Drug combination indicated for the relief of moderate to severe pain.

Class Summary

Some ophthalmologists are advocating that diclofenac (Voltaren) or ketorolac (Acular) drops be used despite lack of official indications. These topical agents have been shown to relieve pain in multiple situations including corneal abrasions, allergies, and postsurgical pain.

Ketorolac tromethamine 0.5% (Acular)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which, in turn, results in reduced inflammation.

Diclofenac ophthalmic (Voltaren)

Inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors.